Ko Takakura (1) and Ikunobu Muramatsu (2,*)
(1) Department of Anesthesiology and Reanimatology, (2) Department of
Pharmacology, Fukui Medical University, Shimoaizuki 23-3, Matsuoka, Fukui
910-1193, Japan
(*) To whom correspondence should be addressed.
Abstract: To investigate whether the nitrergic nerve-mediated
smooth muscle relaxation is caused by authentic nitric oxide (NO) and is
mediated via guanosine 3':5'-cyclic monophosphate (cyclic GMP), we compared
the response to electrical field stimulation of nitrergic nerve (EFS) with
other NO-related responses in rat gastric fundus strips. EFS, sodium nitroprusside
(SNP), S-nitroso-N-acetylpenicillamine (SNAP), and acidified
NaNO2 and inducible NO synthase (iNOS)-mediated NO all produced
relaxation and elevated cyclic GMP level in rat fundus strips. However,
the basal and stimulated cyclic GMP levels were significantly lower than
the basal level in aorta (40+/-4 pmol/g wet tissue). Methylene blue and
6-anilino-5,8-quinolinedione (LY83583), both known as soluble guanylyl cyclase
inhibitors and O2- generators that scavenge NO, reduced
the elevation of cyclic GMP level by all stimuli and ihhibited the relaxations
only in response to NaNO2 and iNOS-mediated NO but not to the
other stimuli. These results suggest that in the rat gastric fundus strips
the relaxations induced by not only nitrergic nerve but also SNP and SNAP
are not associated with cyclic GMP production, in contrast to the relaxations
mediated by authentic NO.
Keywords: Nitric oxide (NO), Nitrergic transmitter, Cyclic GMP, Gastric
fundus (rat), Aorta (rat)